Stress-Induced Fat Storage is the specific metabolic phenomenon where chronic psychological or physiological stress drives a hormonal cascade that preferentially promotes the deposition of visceral adipose tissue, particularly in the abdominal region. This process is mediated primarily by sustained elevation of cortisol, which alters fat cell differentiation and increases the expression of glucocorticoid receptors on adipocytes. This pattern of fat storage is a clinical risk factor for insulin resistance, cardiovascular disease, and metabolic syndrome.
Origin
This concept is a direct link between psychoneuroendocrinology and metabolic health, recognizing that the brain’s perception of stress has a profound and measurable impact on energy partitioning. The term is rooted in the physiological function of cortisol, the primary stress hormone, which mobilizes energy but also redirects its storage. Clinical focus on this term highlights the need to manage stress hormones as a primary strategy for body composition optimization.
Mechanism
The mechanism begins with the chronic activation of the HPA axis, leading to persistent hypercortisolemia, which acts synergistically with insulin to promote adipogenesis. Cortisol up-regulates the enzyme lipoprotein lipase in visceral fat cells, enhancing their capacity to store circulating lipids. This hormonal environment also increases appetite and favors the consumption of calorie-dense comfort foods, creating a positive feedback loop that accelerates the detrimental fat accumulation.
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